The pathogenesis of this disease is inconclusive, a series of observations
and inferences: 1. Mesangial macromolecular uptake excessive study found, to the
exogenous protein in the intravenous injection of the animals tested, can cause
changes similar to the disease, prompted long-term massive proteinuria can lead
to damage of the epithelial cells, mesangial cells over-load to the development
of glomerular focal segmental sclerosis. Glomerular hemodynamic changes in
Benbingfasheng glomerular sclerosis necrosis
High pressure in the glomerular capillary loop role is very important. Studies have shown: the animal model of part or most of nephrectomy, the remaining renal tissue of six months or so that the focal segmental sclerosis. Prompted the disease to occur may be related to hemodynamic changes. The mechanism may be compensatory capillary hypertension in the remaining kidney tissue, as well as the goals, the expansion of the efferent arteriole, glomerular capillary loop completely open to the systemic circulation, resulting in glomerular hyperperfusion, high transmembrane pressure, filtration The increase in protein and other soluble molecules, causing capillary loop epithelial and endothelial cell injury and mesangial cell dysfunction. Given, such as diet control or angiotensin-converting enzyme inhibitor therapy, so that high pressure in the glomerular capillary to reduce the development of focal segmental sclerosis moderated, this is better able to explain the glomerular capillary loop HV role. 3 hyperlipidemia disease, development, and hyperlipidemia was positively correlated. The study found: ① increase in food fat can test animals glomerular sclerosis, glomerular lesions and elevated blood lipids to the same extent. ② congenital growth process of obese rats natural occurrence of focal segmental glomerulosclerosis. ③ to lipid-lowering drug therapy, with the decline in blood lipids, glomerular damage also reduced. Why Does FSGS Relapse and How to Treat it?
(4) human obesity associated with blood cholesterol, triglycerides increased and cardiac hypertrophy, and kidney, there may be similar to the primary focal segmental glomerulosclerosis lesions. Such cases, the control diet, weight loss weight loss, followed by reducing urinary protein nephrotic syndrome can be eased. Hyperlipidemia cause glomerular focal segmental sclerosis may be mesangial cells have the ability to intake of low-density lipoprotein (LDL), oxidized LDL receptor on mesangial cells, and therefore glomerular uptake of oxidized LDL, oxidized LDL is a lipoprotein lead to hardening of the arteries of the most toxic. LDL stimulates mesangial cell proliferation and cell death, leading to glomerulosclerosis. Such as the aforementioned glomerular hemodynamic changes, and high filtration state can lead to glomerular focal segmental sclerosis, and proteinuria. In addition, glomerular lipid deposition is also a focal segmental sclerosis CAUSE. Monocyte-macrophage cells or glomerular mesangial cells engulfed the deposition of LDL to form foam cells (foamcells) and foam cells play an important role in the development of atherosclerosis, so the more support for glomerular focal section segmental sclerosis and atherosclerosis, there is a common pathogenesis. Minimal change disease or membranous nephropathy lipids than the disease is higher, but the glomerular foam cell infiltration are not severe and the disease. Glomerular fat calm can also cause glomerular capillary endothelial cell injury, as well as platelets, macrophages, monocytes, aggregation, stimulate the production of cytokines such as IL-1, TGFβ, etc., these make the mesangial cell proliferation, extracellular matrix components increased and the glomerular capillary lumen clotting. (4) single-macrophages within the glomerular infiltration of mononuclear macrophages can produce a variety of cytokines, such substances to stimulate mesangial cell proliferation leading to glomerulosclerosis. When the monocyte-macrophage cells and histocompatibility antigen (MHC)-positive 1a + cells increase in the number of the disease, the number of these cells with focal segmental sclerosis lesions consistent. The cells and the cell adhesion molecule (ICAM) can activate macrophages, and glomerular macrophage activity. The same time, the monocyte-macrophage cells of the renal interstitial obvious infiltration, the infiltration degree of proteinuria and renal function is consistent with the extent of damage. In addition, the glomeruli of the above-mentioned lesions and cholesterol levels and obesity development process is also relevant. Interstitial mononuclear macrophage infiltration reduce the prednisone treatment, along with improved renal function, but glomerular cell infiltration and sclerosis is difficult to reduce the proteinuria will not improve. Glomerular capillary loop segmental coagulation can activate the platelet release of platelet-activating factor (PAF), platelet-derived growth factor (PDGF), these factors effect caused in the mesangial lesions. Experiments show that the anticoagulant such as heparin, warfarin, or thromboxane inhibitors, can reduce the glomerular focal segmental sclerosis lesions, reduce proteinuria, without affecting renal blood flow and glomerular microscope
Glomerular filtration rate. Plasma factor effect of the disease after renal transplantation can rapidly recurrence, the recurrence rate of up to 35% ~ 50%. Therefore, considering that there may be some plasma factors cause the disease. Some people have in recent years immunoadsorption treatment for the patients and allows urine protein to reduce urinary protein complex l stop adsorption, re-adsorption can still make urine protein decreased, suggesting that the blood of patients with a glomerular capillary loop transparent increase in the material. Visceral epithelial cell lesions occur in the disease development, not only the mesangial matrix plays an important role, and epithelial cells in lesions of the disease starting stove. Pathological observation noted that the onset of the disease both the visceral epithelial cell hypertrophy (hyperplasia), cytoplasm diluted with capillary loop mast, while the filtrate leakage of poor filtration area increases, the formation of false cells. With hypertrophy and dilatation of the capillary loop with fake cell adhesion in the glomerular capsule, forming the start of segmental sclerosis stove On this basis, the development of sclerosis. Genetic factors compatriots, relatives of the disease report few, but there are all the same report of the disease in MHC antigen donor kidney transplant recurrence rate was 82% recurrence rate of 53%, not identical related kidney and other allogeneic donor renal relapse rate of 35% is highly suggestive of genetic factors. In laboratory animals also has the obvious tendency of the germ line.
High pressure in the glomerular capillary loop role is very important. Studies have shown: the animal model of part or most of nephrectomy, the remaining renal tissue of six months or so that the focal segmental sclerosis. Prompted the disease to occur may be related to hemodynamic changes. The mechanism may be compensatory capillary hypertension in the remaining kidney tissue, as well as the goals, the expansion of the efferent arteriole, glomerular capillary loop completely open to the systemic circulation, resulting in glomerular hyperperfusion, high transmembrane pressure, filtration The increase in protein and other soluble molecules, causing capillary loop epithelial and endothelial cell injury and mesangial cell dysfunction. Given, such as diet control or angiotensin-converting enzyme inhibitor therapy, so that high pressure in the glomerular capillary to reduce the development of focal segmental sclerosis moderated, this is better able to explain the glomerular capillary loop HV role. 3 hyperlipidemia disease, development, and hyperlipidemia was positively correlated. The study found: ① increase in food fat can test animals glomerular sclerosis, glomerular lesions and elevated blood lipids to the same extent. ② congenital growth process of obese rats natural occurrence of focal segmental glomerulosclerosis. ③ to lipid-lowering drug therapy, with the decline in blood lipids, glomerular damage also reduced. Why Does FSGS Relapse and How to Treat it?
(4) human obesity associated with blood cholesterol, triglycerides increased and cardiac hypertrophy, and kidney, there may be similar to the primary focal segmental glomerulosclerosis lesions. Such cases, the control diet, weight loss weight loss, followed by reducing urinary protein nephrotic syndrome can be eased. Hyperlipidemia cause glomerular focal segmental sclerosis may be mesangial cells have the ability to intake of low-density lipoprotein (LDL), oxidized LDL receptor on mesangial cells, and therefore glomerular uptake of oxidized LDL, oxidized LDL is a lipoprotein lead to hardening of the arteries of the most toxic. LDL stimulates mesangial cell proliferation and cell death, leading to glomerulosclerosis. Such as the aforementioned glomerular hemodynamic changes, and high filtration state can lead to glomerular focal segmental sclerosis, and proteinuria. In addition, glomerular lipid deposition is also a focal segmental sclerosis CAUSE. Monocyte-macrophage cells or glomerular mesangial cells engulfed the deposition of LDL to form foam cells (foamcells) and foam cells play an important role in the development of atherosclerosis, so the more support for glomerular focal section segmental sclerosis and atherosclerosis, there is a common pathogenesis. Minimal change disease or membranous nephropathy lipids than the disease is higher, but the glomerular foam cell infiltration are not severe and the disease. Glomerular fat calm can also cause glomerular capillary endothelial cell injury, as well as platelets, macrophages, monocytes, aggregation, stimulate the production of cytokines such as IL-1, TGFβ, etc., these make the mesangial cell proliferation, extracellular matrix components increased and the glomerular capillary lumen clotting. (4) single-macrophages within the glomerular infiltration of mononuclear macrophages can produce a variety of cytokines, such substances to stimulate mesangial cell proliferation leading to glomerulosclerosis. When the monocyte-macrophage cells and histocompatibility antigen (MHC)-positive 1a + cells increase in the number of the disease, the number of these cells with focal segmental sclerosis lesions consistent. The cells and the cell adhesion molecule (ICAM) can activate macrophages, and glomerular macrophage activity. The same time, the monocyte-macrophage cells of the renal interstitial obvious infiltration, the infiltration degree of proteinuria and renal function is consistent with the extent of damage. In addition, the glomeruli of the above-mentioned lesions and cholesterol levels and obesity development process is also relevant. Interstitial mononuclear macrophage infiltration reduce the prednisone treatment, along with improved renal function, but glomerular cell infiltration and sclerosis is difficult to reduce the proteinuria will not improve. Glomerular capillary loop segmental coagulation can activate the platelet release of platelet-activating factor (PAF), platelet-derived growth factor (PDGF), these factors effect caused in the mesangial lesions. Experiments show that the anticoagulant such as heparin, warfarin, or thromboxane inhibitors, can reduce the glomerular focal segmental sclerosis lesions, reduce proteinuria, without affecting renal blood flow and glomerular microscope
Glomerular filtration rate. Plasma factor effect of the disease after renal transplantation can rapidly recurrence, the recurrence rate of up to 35% ~ 50%. Therefore, considering that there may be some plasma factors cause the disease. Some people have in recent years immunoadsorption treatment for the patients and allows urine protein to reduce urinary protein complex l stop adsorption, re-adsorption can still make urine protein decreased, suggesting that the blood of patients with a glomerular capillary loop transparent increase in the material. Visceral epithelial cell lesions occur in the disease development, not only the mesangial matrix plays an important role, and epithelial cells in lesions of the disease starting stove. Pathological observation noted that the onset of the disease both the visceral epithelial cell hypertrophy (hyperplasia), cytoplasm diluted with capillary loop mast, while the filtrate leakage of poor filtration area increases, the formation of false cells. With hypertrophy and dilatation of the capillary loop with fake cell adhesion in the glomerular capsule, forming the start of segmental sclerosis stove On this basis, the development of sclerosis. Genetic factors compatriots, relatives of the disease report few, but there are all the same report of the disease in MHC antigen donor kidney transplant recurrence rate was 82% recurrence rate of 53%, not identical related kidney and other allogeneic donor renal relapse rate of 35% is highly suggestive of genetic factors. In laboratory animals also has the obvious tendency of the germ line.
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